Feyza Engin

Credentials: Cellular stress responses, organelle dysfunction and interaction, beta cell function and survival, diabetes

Position title: Associate Professor (also Medicine)

Email: fengin@wisc.edu

Phone: (608) 262-8667

Address:
5214A Biochemical Sciences Building
440 Henry Mall, Madison, WI 53706

The Engin Lab Website

Education

B.S., M.Sc., Istanbul University, School of Pharmacy, 2001
Ph.D., Baylor College of Medicine, 2007
Postdoctoral Fellow, Harvard University, 2013

Honors & Awards

2014 Research Scientist Development Award (K01), NIH/NIDDK
2014 Career Development Award, Juvenile Diabetes Research Foundation
2016 Rising Star in Diabetes, (HeIDi Award) nominee, Novo Nordisk – Helmholtz Diabetes Center
2016 Shaw Scientist Award, Greater Milwaukee Foundation
2018 Finalist, Pathway to Stop Diabetes, Accelerator Award, American Diabetes Association
2021 Invited speaker, joint NIH/NIDDK and Canadian Institute of Health Research (CIHR)-INMD Heterogeneity of Diabetes Symposium (The 100th anniversary of the discovery of Insulin)
2021 Review Editor, Molecular Metabolism
2022 Editorial Board, Diabetes
2022 Editorial Board, Frontier in Endocrinology
2023 Vilas Associate Award, OVCRGE

Research Interests

The endoplasmic reticulum (ER) is a dynamic organelle that plays a key role for cellular homeostasis, development, and stress responsiveness.  In response to cellular stress induced by toxins, unfolded proteins and inflammation, a well-established signaling cascade, the unfolded protein response (UPR), is activated. During UPR, perturbations in ER homeostasis are sensed and transduced by ER membrane localized proteins to the cytoplasm and nucleus to initiate a compensatory response.  While UPR plays a critical role for cell survival during acute stress conditions, hyperactivated UPR or unresolvable stress lead to cell demise. Thus, the unfolded protein response regulates both death and survival effectors. How or when these ER membrane proteins determine whether a cell will survive or die upon ER stress is currently unknown.

We recently showed that, the adaptive functions of the UPR were greatly reduced in β-cells of two different type 1 diabetes (T1D) mouse models and human patients during the progression of T1D. Diabetes incidence in these mouse models was dramatically reduced by mitigating β-cell ER stress with a chemical chaperone. These data suggest that the UPR plays a critical role in β-cell function and survival in T1D. Although this study provides the first direct link between the UPR and T1D pathogenesis and opens the door to a completely novel area of T1D biology, the β-cell specific function of the UPR sensors, their downstream targets, and the molecular mechanisms by which the UPR regulates pancreatic β-cell death/survival during T1D progression still remain largely unknown.

Our laboratory uses biochemistry, cell biology, genetics, -omics and immunology as well as sophisticated genetic and pharmacological tools to understand β-cell specific functions of the UPR sensors, their downstream targets and the molecular mechanisms by which the UPR regulates pancreatic β-cell death/survival.

Publications

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